title: Immunohistological study of lesions induced by Porphyromonas gingivalis in a murine model.
abstract: A previous study used a mouse model to demonstrate protection after challenge with Porphyromonas gingivalis ATCC 33277. In the present study, this same model was used to determine the phenotype of cells recruited into the lesions during the course of the protective immune response after immunization with this periodontal pathogen. BALB/c mice were immunized with 100 micrograms of P. gingivalis outer membrane antigens per mouse weekly for 3 weeks followed by challenge with live organisms 3 weeks after the final immunization. Hematoxylin and eosin-stained sections showed inflammatory infiltrates in all lesions from control (immunized with adjuvant only) and immunized mice. The lesions developed central necrotic cores surrounded by neutrophils, phagocytic macrophages and lymphocytes. Neutrophils were the predominant cells in the lesions 1 day after challenge with significantly more in immunized than control mice. Acid phosphatase and nonspecific esterase-positive macrophages were detected at day 4 and became the predominant cells in the healing lesions. CD4- and CD8-positive T-cells were present from day 1, and while numbers increased over time, there were no significant differences in control or immunized mice. When mice were depleted of CD4 or CD8 cells prior to immunization with P. gingivalis, fewer neutrophils were found in the lesions 1 day after challenge compared with undepleted immunized mice. Acid phosphatase and nonspecific esterase-positive macrophages were not affected by T-cell depletion. The results suggest that the P. gingivalis-induced lesion in immunized BALB/c mice is consistent with a strong innate immune response involving the recruitment of neutrophils in the first instance which may be under the control of T cells. This is followed by the infiltration of phagocytic macrophages which are involved in the healing process and do not appear to be regulated by T cells.
authors.affiliation: Department of Dentistry, University of Queensland, Australia.
authors.forename: E
authors.initials: E
authors.lastname: Gemmell
authors.forename: P S
authors.initials: PS
authors.lastname: Bird
authors.forename: J J
authors.initials: JJ
authors.lastname: Bowman
authors.forename: L
authors.initials: L
authors.lastname: Xu
authors.forename: B
authors.initials: B
authors.lastname: Polak
authors.forename: L J
authors.initials: LJ
authors.lastname: Walsh
authors.forename: G J
authors.initials: GJ
authors.lastname: Seymour
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000942:Antigens, Bacterial / Q000276:immunology; D001425:Bacterial Outer Membrane Proteins / Q000276:immunology; D016516:CD4-CD8 Ratio; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D004195:Disease Models, Animal; D005260:Female; D008262:Macrophage Activation; D008264:Macrophages / Q000201:enzymology / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009504:Neutrophils / Q000201:enzymology / Q000276:immunology; D016966:Porphyromonas gingivalis / Q000276:immunology*; D013997:Time Factors; D014945:Wound Healing / Q000276:immunology
chemical_list: D000942:Antigens, Bacterial; D001425:Bacterial Outer Membrane Proteins